The term "anti-thrombin" was first coined by Morawitz in 1905, and refers to a variety of serum proteins which progressively inactivate thrombin. Hence the term, "anti-thrombin". Anti-thrombin III is one of these anti-thrombins and manifests its effect via interaction with thrombin in circulating blood. This circulating anti-thrombin suppresses the accumulation of thrombin in the circulating system and in that respect acts as an anti-coagulating component. As a result, there is little or no thrombin circulating in the blood of a living host. Were there to be any significant amounts of thrombin, coagulation could begin in vivo and could cause lifethreatening episodes.
When a blood sample is taken from a patient, thrombin formation is initiated via conversion of prothrombin in the presence of calcium ions and the thromboplastin produced by the sampling procedure. The thrombin then acts to convert fibrinogen to fibrin to form a clot. To the extent that anti-thrombin III is present, the formation of thrombin and its effects on the conversion of fibrinogen to fibrin is decreased. Therefore, high levels of anti-thrombin III slow down the coagulation procedure. On PRIOR ART hand, low levels of anti-thrombin III tend to act as pro-coagulants, meaning, of course, that if abnormally short anti-thrombin III assay times are demonstrated by a patient's plasma or serum, that patient may exhibit a predisposition to intra-vascular clotting. While the clinical significance of high levels and low levels of anti-thrombin III varying from the normal ranges has not been fully investigated, there are at least some indications in the literature that low levels are associated with various symptoms of intra-vascular clotting and high levels with symptoms associated with uremic patients and patients on anticoagulant therapy.